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Pathophysiology Thorax > Module #4: Disorders of the Pulmonary System > Flashcards

Module #4: Disorders of the Pulmonary System Flashcards

1
Q

What is hypercapnia?

A

increase PaCO2 in arterial blood

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2
Q

What are some of the causes of hypercapnia?

A

Hypoventilation of alveoli

Supression of respiration centers (DRG/VRG)

Large airway obstructions (tumors/sleep apnea)

Damage to alveoli (emphysema)

Respiratory acidosis

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3
Q

What is tissue hypoxia

A

decreased O2 in ANY tissue

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4
Q

Define Hypoxemia

A

decreased PaO2 in arterial blood

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5
Q

What are the 5 major causes of hypoxemia?

A

Decreased PO2 of inspired air (altitude/suffocation)

Hypoventilation (meds that supress DRG/VRG)

Diffusion abnormality of alveolocapillary membrane (emphysema/fibrosis/edema)

Altered V/Q perfusion ratio (low or high)

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6
Q

What does low V/Q indicative of?

A

good perfusion (blood is getting to lungs fine) but inadequate ventilation

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7
Q

What does he mean by pulmonary “right to left shunting”?

A

Low V/Q

blood travels from RIGHT side of heart and returns to LEFT side of heart w/o receiving O2

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8
Q

What are some clinical examples (diseases) of right to left shunt

A

asthma

chronic bronchitis

pneumonia

ARDS (acute respiratory distress syndrome)

ARDS of infants (hyaline membrane disease

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9
Q

What does high V/Q indicative of?

A

inadequate blood flow in a well ventilated lung

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10
Q

What is a clinical example of a high V/Q?

A

pulmonary embolism

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11
Q

What is pulmonary aspiration?

A

entry of fluids/solids into trachea and lungs

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12
Q

What is pulmonary edema?

A

excess fluid in lungs

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13
Q

What is the most common cause of pulmonary edema?

A

heart disease (increased left sided pressures)

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14
Q

What is atelectasis?

A

collapse of lung tissue

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15
Q

What are the 4 types of atelectasis?

A

Compressive

Absorptive

Surfactant Impairment

Post-Op

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16
Q

What happens to cause compressive atelectasis?

A

external pressure compresses lung

caused by tumors, fluid/air in pleural space (pneumothrorax), abdominal distention

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17
Q

What happens to cause absorptive atelectasis?

A

air from blocked or hypo ventilated alveoli gets absorbed into system

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18
Q

How does surfactant impairment causes atelectasis?

A

lack of surfactant will increase surface tension and makes lungs prone to collapse

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19
Q

How is atelectasis prevented in post-op patients?

A

post-surgical deep breathing exercise

pt positioning

early ambulation (get them up and moving ASAP)

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20
Q

Define pneumothorax

A

air accumulation w/in pleural cavity (pleural space)

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21
Q

What are the 3 types of pneumothorax?

A

Open pneumothorax

Tension pneumothorax

Spontaneous pneumothorax

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22
Q

Describe what happens during an open pneumothorax

A

air enters pleural cavity during inspiration and exits during expiration

air pressure in pleural space now = barometric pressure

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23
Q

Describe what happens during tension pneumothorax

A

air enters plueral cavity during inspiration but DOES NOT EXIT during expiration

there is a gradual build up of air pressure in pleural space, it collapses lung and compresses/displaces other structures of mediastinum (heart/vessels/etc)

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24
Q

Describe what happens during spontaneous pneumothorax

A

an unexpected rupture of pleura

common in 20-40 yo males

may or may not develop into tension pneumothorax

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25
Q

What is pleural effusion?

A

fluid on pleural space

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26
Q

What could pleural effusion cause?

A

compressive atlectasis

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27
Q

What are some causes of fluid buildup?

A

transudate (water)

exudate (protein)

pus (infectious debris)

blood (hemothorax)

lymph fluid (chyle)

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28
Q

Define ARDS

A

acute respiratory distress syndrome due to acute inflammation and alveolar damage

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29
Q

Name some of the causes of ARDS

A

most common causes = infection (sepsis) or multiple trauma

also:

pneumonia

burns

aspiration

cardiopulmonary bypass surgery

pancreatitis

drug OD

smoke/toxic gas inhalation

radiation therapy

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30
Q

What are the 3 pathophysiology phases of ARDS

A

Phase 1: initial injury to lung leads to massive inflammatory response, surfactant is inactivated, alveoli collapse due to less compliance and filling of inflammatory fluid

Phase 2: Hyaline membrane forms into fibrous mass coating alveoli and bronchioles

Phase 3: respiratory failure, secondary systemic (throughout body) inflammatory response; damage other organs which may cause death

31
Q

What are the 3 most common obstructive pulmonary diseases?

A

asthma

emphysema

chronic bronchitis

32
Q

What is going on in the airway with obstructive pulmonary diseases?

A

airway obstruction that is worse w/ expiration

breath out = wheezy

airway expands during inspiration but collapses (recoils) during expiration

33
Q

Name the clinical characteristics of obstructive pulmonary disease

A

Dyspnea = perceived difficulty of breathing

increased work of breathing (WOB)

wheezing

decreased FEV1/FVC ( blood can get to alveoli but lungs can’t deliver O2

34
Q

What is COPD (chronic obstructive pulmonary disease/disorder)?

A

syndrome describes coexisting condition of chronic bronchitis and emphysema

35
Q

What is the primary cause of COPD?

A

smoking

36
Q

What is Chronic Bronchitis?

A

condition of excess mucous secretion and productive cough that lasts 3+ months and occurs 2 consecutive years

37
Q

Describe the Pathophysiology of Chronic Bronchitis

A

bronchial tubes are narrowed –> “traps” air in distal lungs

excess mucous is produced in response to chronic exposure of irritants (smoke, pollution etc)

increased mucous impairs cilia –> increased risk of infection/inflammation

Low V/Q (blood is able to get to alveoli, but air can’t)

Hypoxemia (decreased PaO2 in arterial blood) –> increase in RBC # –> pulmonary hypertension –> cor pulmonale = hypertrophy (enlargement) and failure of right ventricle

Hypercapnia (increased PaCO2)

38
Q

What are the clinical signs/symptoms of Chronic Bronchitis?

A

productive/persistent cough aka smokers cough

recurrent pulmonary infections

reduced flow rates (decreased FEV1/FVC <70%) = prolonged expiration

decreased FVC and increased RV

39
Q

Name the treatments of Chronic Bronchitis

A

Expectorants

Bronchodilators

Physical Therapy (PT) = deep breathing exercises (pursed lip breathing)

Antibiotics and steroids (usually reserved for late stage of disease b/c of side effects)

Low flow O2 to address severe hypoxemia

40
Q

What is the potential adverse effect of low flow O2 for chronic bronchitis?

A

Respiratory Depression

central chemoreceptors (DRG/VRG) are no longer sensitive due to chronic hypercapnia

peripheral receptors have taken over; these guys are sensitive to O2 pressure

if you give to much O2 and PaO2 rises above 60 mmHg, the peripheral receptors will depress ventilation

41
Q

What is emphysema?

A

pathological accumulation of air in the lungs –> enlargement of acini (gas exchange airways)

42
Q

Name and describe the 2 types of emphysema

A

Centriacinar (centrilobar) - destruction of bronchioles/alveolar ducts; alveolar sac remains intact

Panacinar (panlobular) - destruction of ENITRE acinus (terminal bronchiole, alveolar duct, alveoli)

43
Q

Which type of emphysema is more common in chronic smokers?

A

Centriacinar (centrilobar) emphysema

44
Q

Which type of emphysema is more common in the elderly?

A

Panacinar (panlobular) emphysema

45
Q

Describe the pathophysiology of emphysema

A

lung tissue itself is damaged –> breakdown of elastin in septum of bronchioles, alveolar ducts and alveoli

destruction of acinus also damages pulmonary capillary beds

reduced elastin (connective tissue) limits the elastic recoil of lungs –> long slow expiration

46
Q

What are the causes of emphysema?

A

Smoking

47
Q

How does smoking effect the lungs to cause emphysema?

A

smoking inhibits production alpha1-antitrypsin (protease inhibitor) –> promotes the release and accumulation of elastase (enzyme that breaks down elastin (connective tissue protein) –> damages lung tissue

protease = enzyme that breaks down protein in normal tissue alpha1-antitrypsin inhibits elastase

smoking also favors the recruitment of WBC’s in the lungs

48
Q

What are the clinical signs/symptoms of emphysema?

A

Early sign = dyspnea on exertion (DOE)

late sign = dyspnea at rest

NO COUGHING/WHEEZING

prolonged expiration

increased WOB

poor gas exchange –> hypoexmia (decreased PaO2) and hypercapnia (increased PaCO2)

Barrel chest = classic sign

Pts will sit leaned forward with arms extended to breath easier = classic breathing position

Decreased flow rates = FEV1/FVC <70%

FVC decreases

RV/TLC increase

End Stage = pulmonary hypertension and cor pulmonale (just like chronic bronchitis)

49
Q

What are some of the acute treatments for emphysema?

A

O2 therapy

bronchodilators

corticosteroids/antibiotics

50
Q

What are some of the chronic treatments for emphysema?

A

QUIT SMOKING

pulmonary PT –> pursed lipped breathing exercises and safe exercise strategies

O2 therapy (for hypoxemia

Beta agonist (dilate airways)

anticholinergic meds (prevent constriction of airways)

51
Q

What is asthma?

A

reversible obstructive lung disease caused by increased reax of airways to various stimuli (hypersensitive)

52
Q

Describe the pathophysiology of Asthma

A

Initial Attack:

Hyper responsiveness of the airways

stimulus (allergen) triggers massive inflammatory immune response –> inflammation and epithelial damage

3 classic pathological changes: bronchial smooth muscle spasm; mucous production (impair cilia function); vascular congestion

Late asthma response = secondary attack 4-12 hrs after due to infiltration of WBCs; can be more severe than initial attack

53
Q

What are the clinical signs/symptoms of an asthma attack?

A

Audible high pitched wheezing (on either both inspiration and expiration or just expiration)

shortness of breath (SOB)

decreased flow rates (FEV1/FVC <70%)

increased respiration rate (tachypnea)

apprehension/anxiousness (dyspnea, tachycardia, sensation of chest constriction)

early on will have non-productive cough

later on will have productive cough (removes mucous)

54
Q

What are some of the triggers of Asthma attacks?

A

Foods (wines)

Pollen

smoke

dust

mold

animals

pollutants

some are aspirin sensitive (NSAIDs)

Occupational hazards (wood dust, cotton dust, animals, etc)

55
Q

Describe Exercise Induced Asthma (EIA)

symptoms
triggers
duration

A

onset 5 - 15 min after strenuous exercise

triggered especially in dry cold air (late fall)

lasts for 15-60 minutes

can just feel like you’re out of shape

could have “classic” asthma symptoms (SOB, wheezing, chest tightness, anxiety)

worse in “long duration endurace sports”

swimming is better (warm moist air)

56
Q

What are the clinical signs/symptoms of restrictive pulmonary conditions?

A

short shallow breathing patterns

increased or no change in FEV1/FVC (>90%)

Decreased FVC, RV, TLC

dyspnea upon exercise progresses to dyspnea at rest

57
Q

Name the 4 Restrictive Parenchymal Conditions

A

Sarcoidosis

Idiopathic pulmonary fibrosis

Pneumoconiosis

Drug or Radiation-induced interstitial lung disease

58
Q

What is sarcoidosis?

A

inflammation that produces tiny lumps of cells in various organs throughout the body

microscopic lumps = granulomas

59
Q

What are the 7 Restrictive Extraparenchymal Conditions?

A

Myasthenia gravis

Guillain-Barre syndrome

Muscular Dystrophies

C-spine Injuries

Kyphoscoliosis

Obesity

Ankylosing spondylitis

60
Q

What is Pulmonary Fibrosis?

A

excessive fibrosis proliferation in the lungs

61
Q

What are the causes of Pulmonary Fibrosis?

A

secondary complication from disease (TB/ARDS)

inhalation of environmental hazards (pneumoconiosis)

idiopathic pulmonary fibrosis

62
Q

Describe the pathology of pulmonary fibrosis

A

Altered repair process leads to fibrosis and poor lung compliance

chronic inflammation

alveoli are invaded by fibroblasts –> shrink and lose elasticity

63
Q

What is Pneumoconiosis?

A

lung pathology due to inhalation of inorganic environmental hazards (usually chronic exposure)

64
Q

What are the most common inorganic environmental hazards that cause of Pneumoconiosis?

A

Silica –> mining

Asbestos

Coal Miner lung = combo of coal, silica, quartz

65
Q

What causes TB?

A

mycobacterium tuberculosis

66
Q

Describe the pathology of TB

A

inflammatory process is secondary to bacteria

immune response leads to formation of granulomatous lesions (tubercle)

tissue w/in tubercle becomes necrotic (caseous)

scar tissue forms around tubercle

m. tuberculosis remains dormant unless disrupted or if immune system becomes compromised (HIV)

67
Q

What is the single greatest risk factor to reactive TB?

A

HIV

68
Q

How would you diagnose TB?

A

Positive skin test- will indicated pt had disease or was vaccinated

Chest films - see calcifications/nodules in upper lobes of lungs

sputum culture - can take up to 6 wks

69
Q

What is a pulmonary embolism?

A

blood clot

70
Q

How are pulmonary emboli formed?

A

occlusion of pulmonary vascular/capillary supply

71
Q

What happens to V/Q in pt w/ pulmonary embolism and what does that mean?

A

high V/Q ratio

lungs can deliver O2, but blood can’t get to alveoli

72
Q

What is the most common pulmonary embolism?

A

Deep Vein Thrombosis (DVT)

73
Q

What are the pathologic risk factors of pulmonary embolism?

A

Venous stasis - immobility (post-op/being old/travel/obesity), pregnancy, CHF

Hypercoagulation - congenital, oral contraceptives, malignancy

Damage to endothelium of blood vessels - trauma, surgery, CVA (stroke)

74
Q

Describe the Pathology of pulmonary emboli

A

clots, fats, air can form emboli (big old clot)

emboli lodges in lungs

secondary response causes further vasoconstriction –> increase hypoxemia, increase pulmonary blood pressures –> right sided heart failure

vasoconstriction –> decreased surfactant production –> atelectasis –> hypoxemia

if massive enough can lead to cardiac arrhythmias, shock and death

Pathophysiology Thorax (5 decks)

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